*Pain Pathways (Exam II) Flashcards

(67 cards)

1
Q

What are the 2 components of pain?

A
  1. Sensory-discriminative
  2. Motivational-affective

S3

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2
Q

Differentiate the sensory-discriminative & motivational-affective aspects of pain.

A
  • Sensory-discriminative - Ascending pathways and the perception of pain (location, intensity, sensation, etc.)
  • Motivational affective - responses to painful stimuli (Ex. arousal, reflexes, endocrine responses, and emotional changes)

S3

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3
Q

What is nociception?

A
  • The experience of pain through a series of complex neurophysiologic processes.

S4

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4
Q

Medication targets causes of pain through actions on 4 things

A
  1. transduction
  2. transmission
  3. modulation
  4. interpretation

in both PNS and CNS

S4

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5
Q

What is the % of Chronic pain in adult population

A

40 %

(8% - 37% low back pain)

S6

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6
Q

What are the four stages of pain perception?

A
  1. Transduction (tissue level)
  2. Transmission (via nerves)
  3. Modulation (via spinal cord)
  4. Perception (CNS)

S8

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7
Q

What is Transduction?
What 3 types of stimuli turns into action potential?

A

Nerve/electrical impulses/signals start at the nerve endings

Type of stimuli:
- mechanical
- chemical
- thermal

S9 and S10

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8
Q

What is Transmission?
Which nerve fibers are involved?

A

Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.

  • A delta and C fibers

S9 and S10

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9
Q

What is Modulation?

A

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.

S9

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10
Q

What is Perception?
What does it activate?

A

Thalamus acting as the central relay station for incoming pain signals & the primary somatosensory cortex serving for discrimination of specific sensory stimuli.

it activates descending inhibitory pain pathways and memory

S9 and S10

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11
Q

What drugs are used to affect the transduction of pain?
What specifically is being affected by these drugs?

A
  • Local anesthetics & NSAIDs
  • Peripheral nociceptors are affected

S10

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12
Q

What drugs are used to affect the transmission of pain?
What specifically is being affected by these drugs?

A
  • Local anesthetics
  • Αδ and C fibers
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13
Q

What drugs are used to affect the modulation of pain?
What specifically is being affected by these drugs?

A
  • LA’s, opioids, ketamine, α2 agonists
  • Afferent fibers of the dorsal horn

S10

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14
Q

What drugs are used to affect the perception of pain?
What specifically is being affected by these drugs?

A
  • General anesthetics, opioids, α2 agonists
    -Brain

S10

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15
Q

Where does the modulation of pain impulses occur?

A

Dorsal horn of the spinal cord

S12

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16
Q

Where are nociceptors located?

A
  • Skin
  • Muscles
  • Joints
  • Viscera
  • Vasculature

S13

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17
Q

What characterizes afferent C-fibers?

A
  • Unmyelinated
  • Pain from heat (burning) & sustained pressure
  • Slow (less than 2 m/s)

S14

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18
Q

What characterizes A fibers?

A

-Myelinated
- Type I: Aβ & Aδ (heat,mechanical, chemical)
- Type II: Aδ (heat)
- Fast (>2 m/s)

S14

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19
Q

What chemical mediators of pain are targeted with spinal anesthetics?

A

Peptides

  • Bradykinin
  • Calcitonin
  • CGRP
  • Substance P

S15 NEED TO MEMORIZE THIS

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20
Q

Which chemical mediator is released first in response to injury?

A

Bradykinin

S15 NEED TO MEMORIZE THIS

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21
Q

What chemical mediators of pain are inhibited by NSAIDs?

A

Lipids
- Prostaglandins
- Thromboxanes

S15 NEED TO MEMORIZE THIS

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22
Q

What chemical mediators of pain are inhibited by cannabis?

A

Lipids
- Endocannabinoids

S15 NEED TO MEMORIZE THIS

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23
Q

What is sensitization?

A
  • Decreased pain threshold (likely due to upregulation of receptors)

S18

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24
Q

↑ pain sensations to normally painful stimuli.

A

Hyperalgesia

S18

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25
perception of pain to normally non-painful stimuli
Allodynia ## Footnote S18
26
What characterizes primary hyperalgesia?
**Hyperalgesia *at original site* of injury.** - Lower pain threshold - increased response to suprathreshold stimuli - Spontaneous pain - Expansion of receptive field ## Footnote S19
27
What characterizes secondary hyperalgesia?
- Sensitization of CNS → *hyperalgesia from uninjured skin* surrounding injury. ## Footnote S19
28
What is the relay center for nociceptive and sensory activity? How does sensory activity travel from this area to the cerebrum?
- Spinal Dorsal Horn - travels through *Ascending pathways* ## Footnote S20
29
What area of the brain accounts for the perception (location & intensity) of pain?
- Somatosensory Cortex I & II (SI & SII) ## Footnote S20
30
Where are afferent C-fibers located in the spinal column?
- Dorsal horn: Lamina I & II ## Footnote S21
31
What is another name for Lamina II? What drugs work here?
- **Substantia gelatinosa** - *Opioids* work here - also Alpha 2 Agonist (according to Castillo) ## Footnote S21
32
Where are mylinated fibers that innervate muscles and viscera located in the spinal column?
Laminae I, IV, & VII, and ventral horn ## Footnote S21
33
Whichlaminaes are NKI receptor and substance P located in the spinal column?
Laminae III & IV ## Footnote S21
34
What happens when pain is projected to *supraspinal* brain regions
Gate is OPEN ## Footnote S22
35
What happens when pain is not felt with simultaneous inhibitory impulses?
Gate is CLOSE ## Footnote S22
36
What nerve fibers are associated with an "open-gate" for pain? What nerve fibers can shut this gate?
- Aδ & C-fibers = **open** - Aβ fibers = **closed** ## Footnote S22
37
What parts of the brain are involved in the Perception of motivational-affective pain components?
- Limbic cortex - Thalamus ## Footnote S23
38
What areas of the brain may depress or facilitate the integration of painful information in the spinal dorsal horn?
- **PAG** - Peraqueductal Gray Matter - **RVM** - Rostral Ventral Medulla ## Footnote S23
39
What neurotransmitters propagate *excitatory transmissions* in the spinal column?
- Calcitonin - Neuropeptide Y - Glutamate - Aspartate - Substance P ## Footnote S28
40
What neurotransmitters propagate inhibitory transmissions in the spinal column?
- GABAA - Glycine - Enkephalins - NE - Dopamine ## Footnote S28
41
What are the four ascending pain pathways?
- Spinothalamic - Spinomedullary - Spinobulbar - Spinohypothalamic ## Footnote S29
42
What information is carried by the spinothalamic pathway? What laminae are used?
- Pain, Temp, & Itch - Laminae I, VII, and VIII ## Footnote S29
43
What information is carried by the spinobulbar pathway? What laminae are used?
- Behavior towards pain - Laminae I, V, and VII ## Footnote S29
44
What information is carried by the spinohypothalamic pathway? What laminae are used?
- Autonomic, neuroendocrine & emotional aspects of pain - Laminae I, V, VII, & X. ## Footnote S29
45
What part of the suprapinal pathway differentiates where pain is coming from?
Forebrain **S1 & S2** (Somatosensory cortex 1 & 2) ## Footnote S30
46
What supraspinal areas deal with the emotional/motivational aspects of pain?
- Anterior cingulate cortex (ACC) - Insular Cortex (IC) ## Footnote S30
47
Where do the descending inhibitory tracts originate? Where do they then synapse at?
- PAG (periaqeueductal gray matter) - then synapse at dorsal horn ## Footnote S31
48
What neurotransmitters are increased with exercise?
-Serotonin - Endorphins - Enkephalins ## Footnote S31
49
How do inhibitory tracts inhibit the propagation of painful stimuli?
**Hyperpolarizing Aδ & C fibers** - ↓ release of substance P - ↑ pK⁺ and inhibiting Ca⁺⁺ channels ## Footnote S31
50
Descending pathways of pain modulation can be ____ or ____ ?
Inhibited or Faciliated * Descending Inhibition Pathway (DI) * Descending Facilitation Pathway (DF) ## Footnote S32
51
What are factors of Descending Pathways of pain modulation?
* Other somatic stimuli * Psychological factors (arousal, attention, and expectation) ## Footnote S32
52
Where does the pain inhibiting impulse originate from in the descending inhibitory tracts?
PAG-RVM areas ## Footnote S32 and 34
53
When is pain considered *chronic* rather than acute?
- If > 3 - 6 months - If pain persists beyond tissue healing ## Footnote S36
54
Type of pain that persists after the tissue has healed
Neuropathic pain ## Footnote S37
55
Who is at increased risk of neuropathic chronic pain?
- Cancer patients - Diabetics ## Footnote S37
56
What is the treatment for chronic neuropathic pain?
- Opioids - Gabapentin - Cannabis - Amitriptyline *All situation dependent* ## Footnote S37
57
How is visceral pain characterized?
Diffuse and poorly localized ## Footnote S37
58
What is complex regional pain syndrome?
Variety of painful issues following an injury (sponateous pain, hyperalgesia, edema, etc.) ## Footnote S38
59
When can babies begin to perceive pain?
23 weeks | they have lower pain threshold & exaggerated pain responses ## Footnote S38
60
How can the effects of pain in the cardiovascular system be summarized?
- ↑ SNS (↑BP, HR, ↑ SVR, etc.) - Compromised LV ## Footnote S40
61
What are the pulmonary effects of chronic pain?
- ↑ total body O2 consumption/CO2 production - Decreased movement of chest wall (Atelectasis & Intrapulmonary shunting) - Impaired coughing ## Footnote S41
62
How does pain affect the GI/GU system?
- ↑ SNS = ↑ sphincter tone and ↓ peristalsis = **N/V, ileus, distension**, etc. - hypersecretion of acid - Stress ulcers ## Footnote S42
63
What hormones experience an *increase* in response to chronic pain?
**catabolic hormones** *Catecholamines *Cortisol *Glucagon ## Footnote S43
64
What hormones experience a *decrease* in response to chronic pain?
**Anabolic Hormones** - Insulin - Testosterone ## Footnote S43
65
What are Hematologic Response to pain?
**Stress Related** * Platelet adhesiveness * Reduced fibrinolysis * Hypercoagulability ## Footnote S44
66
What are emotional responses to pain?
* Anxiety * Sleep disturbance * Depression ## Footnote S45
67
What are immune responses to pain?
* Stress related Leukocytosis * Depressed reticuloendothelial system Increased infection ## Footnote S45